Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.1.27.4 (
ribonuclease
)
6,621
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Characterising tumour-associated antigens (TAAs) not only represents an important approach to the identification of new diagnostic/prognostic markers, but can also provide information on disease processes and additional potential therapeutic targets. Preliminary screening of a protein macroarray, containing more than 12,000 different proteins, with sera from anaplastic lymphoma kinase (ALK)-negative and ALK-positive anaplastic large cell lymphoma (ALCL) patients identified
ribonuclease
and tumour suppressor protein
Ribonuclease T2
(
RNASET2
), phosphatase lipid phosphate phosphatase-related protein type 3 (LPPR3) and apoptotic adaptor molecule Fas-associating protein (FADD) as ALK-negative ALCL-associated TAAs. Further validation of these observations was confirmed using the ALCL sera in reverse ELISAs. The circulating anti-
RNASET2
autoantibodies present in ALCL patients' sera also recognised eukaryotically expressed
RNASET2
protein.
RNASET2
expression was then investigated in normal tissues and in lymphomas to explore its clinical potential.
RNASET2
protein and mRNA levels showed highest expression in the spleen, leucocytes and pancreas.
RNASET2
protein expression was not restricted to ALK-negative ALCL (81%), being expressed in ALK-positive ALCL (65%) as well as in a number of other lymphomas. The immunological recognition of
RNASET2
, its expression in ALCL and other lymphomas together with its known tumourigenic properties suggest that further studies on this autoantigen are warranted.
...
PMID:RNASET2--an autoantigen in anaplastic large cell lymphoma identified by protein array analysis. 2273 57
Background:
In addition to exploiting its
ribonuclease
capacity,
Ribonuclease T2
(
RNASET2
) has been reported to exert anti-angiogenic and anti-tumorigenic effects in several tumors. However, the role of
RNASET2
in gastric adenocarcinoma (GAC) remains unclear. The purpose of this study was to explore the expression, location, and clinical implications of
RNASET2
in GAC.
Methods:
Data of
RNASET2
mRNA expression in GAC and normal gastric mucosa tissues were extracted from three GSE series and 388 TCGA samples and reanalyzed. Genome-wide CRISPR/Cas9 proliferation screening datasets were used to investigate cell growth changes after
RNASET2
knockout in 19 GAC cell lines. The biological processes involved in
RNASET2
were studied by the bioinformatics analysis. Furthermore, the corresponding experiments including immunohistochemical staining, clinicopathological features analysis, survival curve, microvessel density detection, cell viability assay, and colony formation assay were performed to validate the expression and function of
RNASET2
in GAC.
Results:
An abundance of
RNASET2
was present in the fundus glands and pylorus glands of the normal gastric mucosa.
RNASET2
mRNA and protein were down-regulated in GAC compared with adjacent non-cancerous or normal gastric mucosa tissues. The expression of
RNASET2
mRNA and protein in early GAC was higher than that in advanced GAC. 79/134 gene sets involved in the early GAC pathway were enriched in the
RNASET2
mRNA high expression group. Genome-wide shRNA and CRISPR/Cas9 proliferation screening showed that knockdown or knockout of
RNASET2
could not significantly promote GAC cell growth. AlamarBlue cell viability assay and colony formation assay in AGS cells further validated these results. Clinicopathologic features and survival analysis demonstrated that
RNASET2
protein was significantly correlated with tumor cell differentiation, Lauren's classification, and TM4SF1 protein expression, but not correlated with lymph nodal metastasis and patient's prognosis. Microvessel density detection indicated that no significant correlation was found between the expression of
RNASET2
protein and the angiogenesis of GAC.
Conclusions:
Down-regulation of
RNASET2
in GAC was only the consequence of the GAC, instead of the driver. The expression of
RNASET2
could be regarded as a good biomarker for identifying the early stage of GAC.
...
PMID:Expression, Location, Clinical Implication, and Bioinformatics Analysis of RNASET2 in Gastric Adenocarcinoma. 3252 97
